epigenetics of kidney disease
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This document discusses the epigenetics of kidney diseases. It begins by defining epigenetics as heritable changes in gene expression and phenotype that are not caused by changes in DNA sequence, such as DNA methylation and histone protein modifications. It then focuses on the role of DNA methylation in chronic kidney disease (CKD) and diabetic nephropathy (DN), explaining how hyperglycemia and transforming growth factor beta can induce genes related to apoptosis, fibrosis, and glomerular dysfunction through changes in DNA methylation. Studying the epigenetics of the kidney is important to discover new targeted treatments for kidney diseases, such as inhibitors of DNA methyltransferases and histone deacetylases, which could provide more selective
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- 1. EPIGENETICS OF KIDNEY DISEASES Presented By – RAHUL KUMAR M.Pharm (Pharmaeutics) BITS PILANI 2014H146211P 130/09/2015
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- 3. Learning Objectives • What is epigenetics? • Epigenetic Modification • DNA Methylation • Role of DNA Methylation in kidney disease • Why to study epigenetics CKD? 3
- 4. EPIGENETICS • Epigenetics refers study of heritable changes in gene expression and phenotype that are not mediated by alteration in the underlying DNA sequence of the genome. • Such as • DNA Methylation • Histone Protein Post Transitional Modification 4
- 5. DNA Methylation • DNA methylation is necessary for gene silencing • Enzyme used methyl transferase -DCM (eukaryotes) and DAM (prokaryotes) • Methyl group is obtain from SAM (S- Adenosyl methionine) • DNA Methylation prevent gene expression • CpG islands are hotspot for DNA Methylation 5
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- 7. Role of DNA Methylation in CKD & DN • HG – Hyperglycaemia • TGF-ß Transforming Growth Factor • DNMT • KLF4 Krupple like factor • SIRT 1 -Sirtuin 1 • TF Transcription factor • HMT Histone methyl transferase • HAT Histone methyl transferase HG – Hyperglycaemia TGF-ß Transforming Growth Factor DNMT KLF4 Krupple like factor SIRT 1 -Sirtuin 1 TF Transcription factor HMT Histone methyl transferase HAT Histone acetyl transferase 7
- 8. • DNAme can regulate genes associated with CKD in various renal cells • DNMT 3A & DNMT 3B genes are essential for de-novo methylation • UNC13B gene expression in cortical epithelial cells of kidney upregulated by hyperglycaemia , increase expression of UNC13B gene leads to apoptosis and contributes to renal complications to hyperglycaemia • TGF ß induce expression of PAI 1 (plasminogen activator inhibitor 1 ) contribute to fibrosis 8
- 9. • In fibroblast, the profibrotic TGF ß can promote fibrosis by inhibiting RASAL 1 expression (negative regulator of ras) through promotor hypermethylation leading to generation of fibrosis. • Produces reactive species causes damage to cells • TGF ß promotes SMAD 3 expression (-) wound healing • In normal kidney, KLF 4 regulates DNAme to increase nephrin expression in podocytes 9
- 10. • However, inhibition of KLF 4 expression in disease conditions increases DNAme and inhibit nephrin expression leading to podocyte apoptosis • In contrast, metabolites generated by SIRT 1 in normal epithelial cells promotes claudin- 1 expression in glomerular podocytes via promotor hyper- methylation. • SIRT 1 downregulation under diabetic condition relieves this repression leading to claudin 1 expression and glomerular dysfunction 10
- 11. Why to study epigenetic of Kidney ? • To discover new and better treatments • More selective and specific agents • Eg. HDAC Inhibitors DNMT Inhibitors (under study) Many more to come………………… 11
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